{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T04:04:41Z","timestamp":1787025881251,"version":"build-2736575974"},"reference-count":80,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2016,2,5]],"date-time":"2016-02-05T00:00:00Z","timestamp":1454630400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2016,2,22]]},"abstract":"<jats:p>Although the incidence of Alzheimer\u2019s disease (AD) is continuously increasing in the\n          aging population worldwide, effective therapies are not available. The interplay between\n          causative genetic and environmental factors is partially understood. Meta-analyses have\n          been performed on aspects such as polymorphisms, cytokines, and cognitive training. Here,\n          we propose a meta-analysis approach based on hierarchical clustering analysis of a\n          reliable training set of hippocampus biopsies, which is condensed to a gene expression\n          signature. This gene expression signature was applied to various test sets of brain\n          biopsies and iPSC-derived neuronal cell models to demonstrate its ability to distinguish\n          AD samples from control. Thus, our identified AD-gene signature may form the basis for\n          determination of biomarkers that are urgently needed to overcome current diagnostic\n          shortfalls. Intriguingly, the well-described AD-related genes APP and APOE are not within\n          the signature because their gene expression profiles show a lower correlation to the\n          disease phenotype than genes from the signature. This is in line with the differing\n          characteristics of the disease as early-\/late-onset or with\/without genetic\n          predisposition. To investigate the gene signature\u2019s systemic role(s), signaling pathways,\n          gene ontologies, and transcription factors were analyzed which revealed\n          over-representation of response to stress, regulation of cellular metabolic processes, and\n          reactive oxygen species. Additionally, our results clearly point to an important role of\n          FOXA1 and FOXA2 gene regulatory networks in the etiology of AD. This finding is in\n          corroboration with the recently reported major role of the dopaminergic system in the\n          development of AD and its regulation by FOXA1 and FOXA2.<\/jats:p>","DOI":"10.3233\/jad-150733","type":"journal-article","created":{"date-parts":[[2016,2,23]],"date-time":"2016-02-23T11:42:30Z","timestamp":1456227750000},"page":"1065-1082","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":20,"title":["Meta-Analysis of Transcriptome Data Related to Hippocampus Biopsies and          iPSC-Derived Neuronal Cells from Alzheimer\u2019s Disease Patients Reveals an Association with          FOXA1 and FOXA2 Gene Regulatory Networks"],"prefix":"10.1177","volume":"50","author":[{"given":"Wasco","family":"Wruck","sequence":"first","affiliation":[{"name":"Institute for Stem Cell Research and Regenerative Medicine, Heinrich-Heine-Universit\u00e4t D\u00fcsseldorf, D\u00fcsseldorf,\r            Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Friederike","family":"Schr\u00f6ter","sequence":"additional","affiliation":[{"name":"Institute for Stem Cell Research and Regenerative Medicine, Heinrich-Heine-Universit\u00e4t D\u00fcsseldorf, D\u00fcsseldorf,\r            Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James","family":"Adjaye","sequence":"additional","affiliation":[{"name":"Institute for Stem Cell Research and Regenerative Medicine, Heinrich-Heine-Universit\u00e4t D\u00fcsseldorf, D\u00fcsseldorf,\r            Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2016,2,5]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.3389\/fneur.2015.00038"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jalz.2012.11.007"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/ng1934"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.8346443"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10522-008-9197-8"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10522-009-9219-1"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1177\/193229680800200619"},{"key":"e_1_3_3_9_2","first-page":"5","article-title":"The interplay between metabolic homeostasis and\n            neurodegeneration: Insights into the neurometabolic nature of amyotrophic lateral\n            sclerosis","volume":"4","author":"Ngo ST","year":"2015","unstructured":"NgoST, SteynFJ (2015) The interplay between metabolic homeostasis and neurodegeneration: Insights into the neurometabolic nature of amyotrophic lateral sclerosis. 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